The biochemical mechanism by which series E prostaglandins (PGE) and Beta-adrenergic catecholamines (Beta-agonists) exert their powerful but diametrically opposed effects on uterine smooth muscle cells are being investigated at the adenylate cyclase level. Enzyme stimulation by PGE but not Beta-agonist is sensitive to the inhibitory effects of the Na plus over the physiologic concentration range. This Na plus sensitivity may explain the inhibitory effect PGE has on Beta-agonist-dependent cAMP production by intact muscle strips since an important initial event in excitation-concentration coupling is an inward directed Na plus current which contributes to depolarization of the sarcolemma. The mechanism of Na plus inhibition will be investigated at the level of the guanylyl nucleotide-requiring step which couples hormone receptors and the adenylate cyclase catalytic subunit in hormone target tissues in general and which is shared by the PGE and B-agonist receptor in the uterine smooth muscle cell. The results from this investigation will then be applied to investigations of the effects of oxytocin, the potent smooth muscle contractile agent which, like PGE, has been shown to inhibit cAMP responses in the uterine smooth muscle cell.